Low maternal hemoglobin during pregnancy and diminished neuromotor and neurocognitive performance in offspring with schizophrenia

Department of Psychology, Temple University, Philadelphia, PA, USA.
Schizophrenia Research (Impact Factor: 3.92). 06/2012; 138(1):81-7. DOI: 10.1016/j.schres.2012.04.008
Source: PubMed


Previous research has linked maternal anemia during pregnancy with increased risk for schizophrenia in offspring. However, no study has sought to determine whether this early insult leads to a more severe form of the disorder, characterized by worsened motor and neurocognitive functioning.
Subjects were 24 cases diagnosed with schizophrenia and 22 controls from the Developmental Insult and Brain Anomaly in Schizophrenia (DIBS) study. Hemoglobin values were measured throughout pregnancy. Among offspring, psychiatric diagnoses were determined through semi-structured interviews and medical records review and comprehensive neurocognitive assessment batteries were conducted in adulthood.
Results indicated that among cases decreases in maternal hemoglobin led to significant decreases in scores on the Grooved Pegboard test, the Finger Tapping test and the Wechsler Adult Intelligent Scales (WAIS) information subtest. In contrast, controls only exhibited decreases in performance on the California Verbal Learning Test (CVLT) long-delay recall after fetal exposure to lower hemoglobin. There were also significant interactions between hemoglobin and case status for all of the motor tasks.
These findings support the hypothesis that fetal exposure to decreases in maternal hemoglobin is related to preferentially poorer neuromotor function among cases compared to controls, as well as general intellectual difficulties among cases. Controls were relatively unaffected by decreased maternal hemoglobin, which suggests that liability to schizophrenia renders cases susceptible to the deleterious influences of in utero exposure to decreases in maternal hemoglobin.

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    ABSTRACT: Objective: Schizophrenia is associated with excess physical comorbidity. Yet, to our knowledge, large studies are lacking on the associations with somatic diseases before the onset of schizophrenia. The authors conducted a nationwide study of the full spectrum of treated somatic diseases before the first diagnosis of schizophrenia. Method: Nationwide sample of the Danish population consisting of singletons (n = 954351) born 1977-1993 and followed from birth to 2009, during which period 4371 developed schizophrenia. Somatic diagnoses at all general hospital contacts (admitted or outpatient care at a somatic hospital) from 1977 to 2009 were used as exposures. The incidence rate ratio (IRR) of schizophrenia was calculated using Poisson regression adjusted for confounders. Results: Among the 4371 persons who developed schizophrenia from 1992 to 2009, a total of 4180 (95.6%) persons had a previous somatic hospital contact. A history of any somatic hospital contact was associated with an elevated risk of schizophrenia (IRR = 2.04, 95% CI = 1.77-2.37). A wide range of somatic diseases and conditions were associated with an increased risk of schizophrenia, including epilepsy (IRR = 2.26, 95% CI = 1.93-2.62), nutritional or metabolic disorders (IRR = 1.57, 95% CI = 1.39-1.77), circulatory system diseases (IRR = 1.63, 95% CI= 1.38-1.92), and brain injury (IRR = 1.58, 95% CI = 1.45-1.72). Conclusions: A wide range of potential etiological factors could have contributed to the observed associations, including genetic or physiological overlaps between conditions, and interacting immunological, behavioral, and neurodevelopmental factors.
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